In Parkinson's disease, the death of the midbrain dopamine neurons induces a decrease in the amount of dopamine released into the striatum, disrupting the balance between dopamine and acetylcholine in the striatum, thereby developing dyskinesia.
It has also been confirmed that Parkinson's disease is caused by oxidative stress and inhibition of mitochondrial complex I (Nonpatent Publications 1 to 3), suggesting that Parkinson's disease can be treated by suppressing oxidative stress and inhibition of mitochondrial complex I.
Currently employed methods for the treatment of Parkinson's disease are divided roughly into four as follows.    1) Dopamine replacement therapy. Since dopamine itself has low blood-brain barrier (BBB) permeability, L-dopa (levodopa), a dopamine precursor that has a high BBB permeability, is administered. Although L-dopa exhibits an excellent effect at initial stages of administration, L-dopa itself may give an oxidative stress on neurons, and may adversely aggravate the symptoms.    2) Administration of a drug that suppresses the dopamine degradation system. For example, selegiline is known as a drug for inhibiting monoamine oxidase, MAO, which is involved in dopamine degradation.    3) Administration of a drug that activates dopamine transporter, which is present at the striatum membrane and has the function of uptaking dopamine into the striatum.    4) Administration of a drug (such as trihexyphenidyl) that suppresses the acetylcholine production by suppressing the function of cholinergic neurons in a hyperexcited state.
However, since these therapeutic methods are palliative treatments for the decrease in the amount of dopamine due to neuronal death, there is a desire for a therapeutic method that suppresses neuronal death itself.
DJ-1 protein, on the other hand, is present in a wide range of human cells including neurons, and consists of 189 amino acids. DJ-1 protein is an oncogene product, being known to be involved in PARK7 (familial Parkinson's disease) (Nonpatent Publication 4).
Furthermore, it is known that DJ-1 protein has an effect in suppressing neuronal death caused by oxidative stress. It has been reported that, when a Parkinson's disease model rat that has been injected with 6-hydroxydopamine, which gives oxidative stress, is injected with DJ-1 protein simultaneously with or after the injection of the 6-hydroxydopamine, the death of dopamine neurons is suppressed, and behavioral abnormality is improved (Nonpatent Publication 5).
It has also been reported that a DJ-1 protein C106 variant (106th amino acid residue being altered from cysteine to serine) does not suppress the death of dopamine neuronal in a Parkinson's disease model rat (Nonpatent Publications 6 and 7).    [Nonpatent Publication 1]    Neurochem. Res. 2004 March, 29 (3); 569-577    [Nonpatent Publication 2]    Neurochem. Res. 2003 October, 28 (10); 1563-1574    [Nonpatent Publication 3]    Annals of Neurol. 1996 October, 40 (4); 663-671    [Nonpatent Publication 4]    Science, 2003 January, 299 (5604); 256-9    [Nonpatent Publication 5]    Experimental Neurology, 2002, 175; 303-317    [Nonpatent Publication 6]    EMBO Reports, 2004 February, 5 (2); 213-8.    [Nonpatent Publication 7]    Biochem. Biophys. Res. Commun., 2004 Jul. 23, 320 (2); 389-97.